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Biomedical subjects

N Nathanson

Publications and source records attributed to N Nathanson.

At least 109 records · Page 6Linked to original sources
PubMed1972

Immunopathogenesis of acute central nervous system disease produced by lymphocytic choriomeningitis virus. I. Cyclophosphamide-mediated induction by the virus-carrier state in adult mice.

A single dose of 150 mg/g of cyclophosphamide (CY), given 3 days after intracerebral (i.c.) inoculation of lymphocytic choriomeningitis (LCM) virus, protected over 90% of adult BALB/c mice against acutely fatal choriomeningitis. Surviving mice became persistently infected carriers, with high virus titers in blood and brain. Immunofluorescent examination of the brain showed that in CY-induced carriers infection was initially confined to the choroid plexus, ependyma, and leptomeninges, but over the next 30 days gradually spread to the neural parenchyma, most notably to the molecular layer of the cerebellum. By contrast, LCM virus-carrier mice produced by neonatal virus injection and examined as adults, showed a much less marked infection of choroid plexus and much more widespread infection of parenchyma, with a different distribution among brain nuclei, including heavy infection of the Purkinje cells of the cerebellum.

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PubMed1972

Immunopathogenesis of acute central nervous system disease produced by lymphocytic choriomeningitis virus. II. Adoptive immunization of virus carriers.

Lymphocytic choriomeningitis (LCM) virus carriers were established by intracerebral inoculation of adult BALB/c mice followed by a single dose of cyclophosphamide (CY) (150 mg/kg) 3 days after infection, and by intracerebral injection within 24 hr of birth. These carriers were then adoptively immunized with spleen cells or serum from immune or normal BALB/c donors. Transfer of immune spleen cells into drug-induced carriers consistently resulted in acutely fatal choriomeningitis, histologically strikingly similar to classical LCM. Normal spleen cells or immune serum failed to produce either central nervous system (CNS) pathology or illness with any regularity. In addition, focal necrosis of the cerebellum was seen after adoptive immunization of drug-induced carriers but only when mice received cells at least 3 wk after inoculation, which is probably explained by the gradual spread of infection from membranes to the neural parenchyma during the first month after establishment of the carrier state in adult mice. Immune spleen cells, when transferred to neonatal carriers, led to a decrease in virus titers in blood and brains and to development of antibody without acute CNS disease. It appears that the production of fatal choriomeningitis after LCM infection is determined in part by the distribution of viral antigen, and this is markedly different in neonatal and drug-induced carriers at the time of cell transfer. Another factor of potential importance is the much higher level of circulating viral antigen in the plasma of neonatal than in that of drug-induced LCM carriers. Classical LCM disease can only be transferred by immune lymphoid cells and not by antiserum. Furthermore, little or no complement-fixing (CF) antibody was found in the plasma of mice dying of acute choroiditis. These observations strongly suggest that acute choroiditis is dependent upon the cell-mediated immune response.

Animals↗
PubMed1971

Effect of antilymphocyte serium on tacaribe virus infection in infant mice.

Tacaribe virus, a member of the arenovirus group, was demonstrated to have similarities in pathogenesis to the prototype virus of this group, lymphocytic choriomeningitis (LCM) virus. Treatment with antilymphocyte serum (ALS) doubled the survival time of mice neonatally infected with a lethal dose of Tacaribe virus. Twenty-one per cent of ALS-treated infected animals survived more than 30 days. All animals had recoverable virus in brains and serum for the duration of life, and there was no difference between virus growth curves of ALS-treated and control animals. No neutralizing or complement-fixing antibodies were present in infected animals at time of death, with the exception of one long-surviving ALS-treated animal. Certain differences between infections of mice with LCM and Tacaribe viruses were apparent. Tacaribe virus pathogenicity decreased with increasing mouse age, and earlier infection and a more prolonged course of ALS treatment than was needed for LCM virus were necessary to achieve increased survival. Histopathological changes observed in Tacaribe virus-infected control mice were focal choroiditis and focal cerebellar necrosis; these changes were not seen in asymptomic infected mice during the period of transient protection by ALS.

Journal Article↗
PubMed1970

Experimental encephalitis following peripheral inoculation of West Nile virus in mice of different ages.

Experimental arbovirus infections of mice provide a convenient model to study factors which determine the occurrence or severity of encephalitis following extraneural infection with certain neurotropic viruses. Varying doses of West Nile or Powassan viruses were inoculated by intraperitoneal or intramuscular routes into mice of varing ages; individual variables were manipulated to influence the outcome of infection. Three patterns of pathogenesis were delineated: (1) Fatal encephalitis, preceded by early viraemia, and invasion of the central nervous system. (2) Inapparent infection, with no detectable viraemia and no evidence of central nervous system invasion. (3) Subclinical encephalitis, usually preceded by trace viraemia, with minimal transient levels of virus in the brain. In this latter type of subclinical infection with a potentially lethal virus, the immune response probably plays an important role in recovery.

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